Purpose: Galectin (Gal)-1, an endogenous lectin found at sites of immune privilege, plays a critical role in the regulation of the immune response. Therapeutic administration of Gal-1 or its genetic delivery suppresses chronic inflammation in experimental models of autoimmunity. The purpose of this work was to investigate the occurrence of circulating anti-Gal-1 antibodies in patients with autoimmune and infectious uveitis as potential determinant factors of disease progression.
Methods: IgG, IgE, and IgA anti-Gal-1 antibodies were assessed by ELISA and Western blot in sera from patients with autoimmune (n = 47) and infectious (n = 15) uveitis compared with healthy control subjects (n = 30). The frequency of anti-Gal-1 antibodies was examined in patients experiencing poor clinical outcome (n = 21) or good evolution (n = 9). Anti-Gal-1 antibodies were eluted by incubating patient sera with nitrocellulose filters adsorbed with rGal-1. The ability of these antibodies to recognize retinal tissue was assessed by ELISA, Western blot, and immunohistochemistry.
Results: IgE, IgG, and IgA anti-Gal-1 antibodies were increased in sera from patients with autoimmune uveitis (P < 0.001 vs. controls) and toxoplasmic retinochoroiditis (P < 0.001). The level of anti-Gal-1 IgE and IgG antibodies was associated with progressive disease and poor outcome in autoimmune and infectious uveitis. Furthermore, these antibodies strongly immunoreacted with retinal lysates and recognized retinal structures mainly photoreceptors in retinal sections.
Conclusions: Anti-retinal Gal-1 antibodies are present in sera from patients with uveitis and can be associated with the progression of ocular disease, suggesting their potential use in follow-up observations of these patients.